Abstract
We observed a consistent eye-open at birth (EOB) phenotype in mouse pups homozygous for a leucine-rich repeat containing G-protein coupled receptor 4 (Lgr4) allele deleting the whole transmembrane domain coding region. An in vitro wound-healing scratch assay showed notably reduced keratinocyte motility in the null mice. Phalloidin staining of F-actin in the eyelid epidermis was also reduced. We also generated keratinocyte-specific Lgr4 deficient mice, circumventing the embryonic/neonatal lethality and kidney abnormalities. Most of the conditional Lgr4 knockout mice showed the EOB phenotype. Thus, Lgr4 might be a novel gene class regulating cell motility.
| Original language | English |
|---|---|
| Pages (from-to) | 4685-4690 |
| Number of pages | 6 |
| Journal | FEBS Letters |
| Volume | 581 |
| Issue number | 24 |
| DOIs | |
| Publication status | Published - 2007 Oct 2 |
Keywords
- EOB
- GPCR
- GPR48
- Gene deletion mice
- Keratinocyte
- LGR4
ASJC Scopus subject areas
- Biophysics
- Structural Biology
- Biochemistry
- Molecular Biology
- Genetics
- Cell Biology
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Kato, S., Mohri, Y., Matsuo, T., Ogawa, E., Umezawa, A., Okuyama, R., & Nishimori, K. (2007). Eye-open at birth phenotype with reduced keratinocyte motility in LGR4 null mice. FEBS Letters, 581(24), 4685-4690. https://doi.org/10.1016/j.febslet.2007.08.064